Sinapic acid attenuates X-ray-induced hippocampal injury by suppressing oxidative stress, neuroinflammation, apoptosis, and NLRP3-mediated pyroptosis

Abstract

AimIonizing radiation, while essential for managing brain tumors, often damages healthy hippocampal tissue and impairs cognitive function. The present study investigated whether sinapic acid, a naturally occurring phenolic compound, could protect the rat hippocampus from X-ray–induced injury and explored the underlying mechanisms.MethodsAdult male Wistar rats were assigned to four groups: control, sinapic acid alone (40 mg/kg orally), whole-body X-ray irradiation (8 Gy), and sinapic acid pretreatment followed by irradiation. Hippocampal tissue was collected 48 hours post-exposure for biochemical and histological analysis.ResultsX-ray exposure severely disrupted redox balance, as evidenced by reduced Nrf2 and HO-1 levels, diminished activities of SOD, CAT, and GPx, and elevated MDA concentrations. Irradiation also triggered a robust inflammatory response characterized by NF-κB activation and increased TNF-α, IL-6, and interleukin-1 beta. Furthermore, radiation promoted programmed cell death through both pyroptotic (NLRP3, caspase-1, gasdermin-D) and intrinsic apoptotic (caspase-9, cytochrome c, caspase-3, Bax) pathways. These molecular disturbances corresponded with extensive neurodegeneration in the hippocampal CA3 region. Remarkably, sinapic acid pretreatment significantly reversed these detrimental effects. It restored Nrf2/HO-1 signaling, reinstated antioxidant enzyme function, suppressed NF-κB–driven inflammation, and reduced markers of both pyroptosis and apoptosis. Histological examination confirmed that sinapic acid preserved CA3 pyramidal neuron architecture.ConclusionThe results demonstrate that sinapic acid provides robust neuroprotection against radiation-induced hippocampal damage through simultaneous activation of antioxidant defenses, inhibition of inflammatory cascades, and blockade of cell death pathways.

Keywords

Introduction

X rays are a form of electromagnetic ionizing radiation composed of massless photons capable of ejecting electrons from biological molecules, thereby disrupting normal cellular processes.¹ Although X ray–based cranial irradiation is a cornerstone in the treatment of primary and metastatic brain tumors, its therapeutic benefits are often accompanied by unintended injury to surrounding healthy tissue. Among the most concerning complications is cognitive impairment, which can markedly diminish patients’ quality of life.² A substantial body of evidence indicates that these adverse effects are largely driven by the generation of free radicals, which initiate oxidative injury. Consequently, antioxidant compounds have been widely explored for their potential to counteract radiation induced cellular damage by scavenging reactive species.³
Sinapic acid, a hydroxycinnamic acid derivative belonging to the phenolic acid family, is an orally bioavailable phytochemical abundant in spices, fruits, vegetables, cereals, and oilseed crops.⁴ Increasing evidence highlights its diverse pharmacological properties, including neuroprotective activities.⁵ Sinapic acid has been shown to exert potent antioxidant, antiproliferative, and anti-apoptotic effects.6 Its antiapoptotic actions involve suppression of pro apoptotic proteins such as Bax and caspase 3, coupled with enhanced expression of the anti apoptotic protein Bcl 2.⁶ In terms of inflammation, sinapic acid inhibits NLRP3 inflammasome activation, reduces caspase 1 activity, and lowers IL 1β production in both in vivo and in vitro models.⁷ It also decreases oxidative and inflammatory markers including MDA, tumor necrosis factor α, and myeloperoxidase in experimental models of inflammatory bowel disease.⁸ Furthermore, sinapic acid suppresses NF κB signaling and its downstream inflammatory mediators, as demonstrated in doxorubicin induced cardiotoxicity.⁶
Given this broad spectrum of antioxidant, anti inflammatory, and antiapoptotic activities, the present study was undertaken to evaluate the neuroprotective potential of sinapic acid against X ray–induced hippocampal injury, with particular emphasis on its ability to counteract oxidative stress, inflammatory signaling, and programmed cell death.

Materials and Methods

AnimalsForty adult male Wistar rats weighing 150–200 g were used in this experiment. Before initiating the study, all animals were allowed a one week acclimation period to adjust to the laboratory environment. Throughout both the acclimation and experimental phases, the rats were provided unrestricted access to standard rodent chow and tap water. They were housed in polypropylene cages under controlled environmental conditions, including a 12:12 hour light–dark cycle, a temperature of 23 ± 1 °C, and relative humidity maintained between 30% and 35%.Experimental DesignFollowing the one week acclimatization period, the forty rats were randomly allocated into four groups of equal size according to the planned treatment protocol. The sample size per experimental group was established through a prospective power calculation performed with G*Power software with an anticipated effect magnitude of 1.2, a Type I error threshold of 0.05, and a target statistical power of 0.80. Group I (Control): Animals received 0.5 mL of normal saline orally. Group II (Sinapic acid alone): Rats were administered sinapic acid at a daily oral dose of 40 mg/kg, as described by Ahmad et al..⁹ The compound was purchased from Sigma Aldrich (St. Louis, MO, USA). Group III (X ray irradiation): Animals were subjected to whole body X ray exposure at a total dose of 8 Gy, following the method of Hussein et al. (2006). Group IV (Sinapic acid + X ray): Rats received sinapic acid orally (40 mg/kg/day) one hour prior to whole body irradiation, using the same radiation protocol as Group III.¹⁰
All animals were euthanized 48 hours after irradiation using thiopental sodium anesthesia (30 mg/kg). Brains were immediately excised and divided into two equal halves. One half was coronally sectioned and fixed in 10% neutral buffered formalin for histological evaluation of the hippocampus, while the remaining half was stored at −80 °C for subsequent biochemical analyses.Hematoxylin and Eosin (H&E) StainingAfter collection, hippocampal tissues were immediately fixed in 10% neutral buffered formalin for 24 hours. The fixed specimens were rinsed and processed through a graded ethanol series for dehydration, followed by xylene clearing and paraffin embedding. Paraffin blocks were sectioned at 5 µm thickness, and the sections were mounted onto glass slides. Routine H&E staining was performed, after which the stained slides were examined under a light microscope for morphological assessment.Evaluation of Oxidative Stress ParametersThe levels of oxidative stress indicators in hippocampal homogenates were determined using ELISA kits following the factory guidelines. Specifically, the kits measured MDA (Cat. No. E0156Ra, sensitivity: 0.05–10 nmol/mL), SOD (Cat. No. E1444Ra, 0.05–30 ng/mL), CAT (Cat. No. E0869Ra, 1–300 ng/mL), GPx (Cat. No. E1172Ra, 0.5–200 ng/mL), Nrf2 (detection window: 0.2–60 ng/mL), and (HO-1; Cat. No. E0676Ra, 0.05–20 ng/mL).
Evaluation of Inflammatory, Pyroptotic, and Apoptotic Parameters
The levels of inflammatory, pyroptotic, and apoptotic markers in hippocampal homogenates were quantified using ELISA kits in accordance with the manufacturers' instructions. Inflammatory indices assessed included NF-κB (Cat. No. E2182Ra; 10–2000 ng/L), TNF-α (Cat. No. E0764Ra; 5–1000 ng/L), IL-1β (Cat. No. E0119Ra; 0.2–60 ng/mL), and IL-6 (Cat. No. OKBB0019; 62.5–4000 pg/mL). Pyroptosis-related markers measured were NLRP3 (Cat. No. NBP3-42294; 0.312–20 ng/mL), caspase-1 (Cat. No. NBP2-75015; 62.50–4000 pg/mL), and gasdermin-D (GSDMD; Cat. No. MBS9356357; 0.625–20 ng/mL). Apoptotic markers evaluated included caspase-3 (Cat. No. NBP2-75024; 0.31–20 ng/mL), caspase-9 (Cat. No. CSB-E08863r; 62.5–4000 pg/mL), and cytochrome c (Cat. No. ABIN6955222; 1.56–100 ng/mL).Real-Time Quantitative Polymerase Chain ReactionExpression of the pro apoptotic gene Bax and the reference gene β actin was quantified in rat brain tissue using real time quantitative PCR. Amplification reactions were performed on an Applied Biosystems StepOnePlus system. Total RNA was isolated from brain samples using a Qiagen RNA extraction kit according to the manufacturer’s instructions. The resulting RNA was reverse transcribed into cDNA using the Sense Fast cDNA synthesis kit. Data collection and analysis were carried out with Applied Biosystems software. The primer sequences used were: as follows: Bax forward 5′-CACGTCTGCGGGGAGTCA-3′ (GenBank NM_017059), Bax reverse 5′-TAGGAAAGGAGGCCATCCCA-3′; β-actin forward 5′-CCGTAAAGACCTCTATGCCA-3′ (GenBank NM_031144), and β-actin reverse 5′-AAGAAAGGGTGTAAAACGCA-3′.Ethical ApprovalThe experimental procedures involving animals were reviewed and approved by the Research Ethics Committee of Umm Al-Qura University, Makkah, Saudi Arabia (Date: 2026-1-29; Reference No.: HAPO-02-K-012-2026-05-3491).Statistical AnalysisAll data are presented as mean ± (SD). Before proceeding with any comparative analyses, we evaluated the distribution pattern of our datasets using the Shapiro–Wilk test. Comparisons among the experimental groups were performed using (ANOVA), followed by the Tukey–Kramer post hoc test to determine pairwise differences. Statistical analyses and graph preparation were conducted using GraphPad Prism software (version 8; ISI®, USA). A p value of less than 0.05 was considered statistically significant.Reporting GuidelinesThe study was conducted in full accordance with the ARRIVE guidelines to ensure transparency and reproducibility in animal research.

Results

Antioxidant Effect of Sinapic AcidExposure to 8 Gy X ray irradiation markedly suppressed the Nrf2/HO 1 antioxidant pathway in hippocampal tissue, as evidenced by an 84% reduction in Nrf2 and an 81% reduction in HO 1 relative to the control group. This downregulation was accompanied by a profound decline in endogenous antioxidant defenses, with GPx, SOD, and CAT decreasing by 84%, 61%, and 79%, respectively, compared with normal animals. Consistent with this oxidative imbalance, MDA levels exhibited a 446% elevation following irradiation (Figure 1A-F).
Oral administration of sinapic acid (40 mg/kg) prior to irradiation significantly counteracted these alterations. Combined treatment restored Nrf2 by 144% and HO 1 by 149% relative to the X ray group. Likewise, sinapic acid markedly enhanced antioxidant enzyme activities, increasing GPx by 255%, SOD by 67%, and CAT by 206%, while reducing MDA levels by 55% compared with irradiated rats. Collectively, these findings confirm the potent antioxidant capacity of sinapic acid and its ability to mitigate X ray–induced oxidative injury in experimental rats.Sinapic Acid Preserves Hippocampal MorphologyFigure 2 demonstrates the structural alterations observed in the CA3 pyramidal layer following X ray exposure. Rats subjected to irradiation showed pronounced neurodegenerative changes, including neuronal shrinkage, dense cytoplasmic condensation, and clear disruption of pyramidal cell architecture. These abnormalities were not present in the
control or sinapic only groups. Co administration of sinapic acid markedly alleviated the X ray–induced damage, restoring the CA3 region toward its normal cytoarchitecture and highlighting the compound’s strong neuroprotective potential.Anti Inflammatory Character of Sinapic AcidX ray irradiation induced a pronounced neuroinflammatory response in hippocampal tissue, reflected by a 1051% rise in NF κB and marked elevations in pro inflammatory cytokines, including TNF α (903%), IL 6 (441%), and IL 1β (538%) compared with the control group. Pretreatment with sinapic acid effectively attenuated this inflammatory surge, reducing NF κB by 67%, TNF α by 69%, IL 6 by 56%, and IL 1β by 38% relative to irradiated rats (Figure 3A-D).Sinapic Acid Attenuates X ray–Induced Hippocampal Pyroptosis and ApoptosisX ray irradiation triggered a pronounced activation of pyroptotic signaling in hippocampal tissue, reflected by sharp increases in NLRP3 (788%), caspase 1 (756%), and GSDMD (335%) compared with control rats. Concurrently, intrinsic apoptotic markers were markedly elevated, including caspase 3 (624%), caspase 9 (556%), cytochrome c (488%), and Bax (414%), confirming extensive neuronal injury.
Pretreatment with sinapic acid substantially mitigated these effects, reducing NLRP3 by 63%, caspase 1 by 45%, GSDMD by 54%, caspase 3 by 49%, caspase 9 by 49%, cytochrome c by 41%, and Bax by 53% relative to irradiated rats (Figure 3E-K).

Discussion

Cranial irradiation remains a cornerstone in the management of primary and metastatic brain tumors, yet its therapeutic benefits are often accompanied by adverse effects, including cognitive decline that can markedly diminish patients’ quality of life.^1,2 The present study aimed to evaluate the radioprotective potential of sinapic acid, a well recognized antioxidant, against hippocampal injury induced by X ray exposure in rats, while elucidating the underlying molecular mechanisms. Our findings demonstrate that administering sinapic acid at 40 mg/kg effectively preserved the structural integrity of the CA3 region following 8 Gy irradiation. This protection was associated with reduced hippocampal lipid peroxidation, restoration of endogenous antioxidant defenses through Nrf2 pathway activation, attenuation of irradiation induced neuroinflammation, suppression of pyroptotic inflammasome formation, and a marked decrease in neuronal apoptosis.
As an ionizing radiation source, X rays induce molecular dissociation that directly damages critical macromolecules such as DNA.¹¹ In parallel, they ionize intracellular water, generating reactive oxygen species (ROS) that amplify cellular injury.¹² These ROS attack lipids, proteins, and nucleic acids, initiating oxidative stress and activating inflammatory and apoptosis related pathways that ultimately culminate in cell death.¹³ Our findings align with these mechanisms, as X-ray produced marked oxidative damage in hippocampal tissue, reflected by elevated MDA levels and significant reductions in GPx, CAT, and SOD compared with control rats. These results are consistent with earlier work by Erol et al.,¹⁴ who reported substantial increases in MDA following 7.2 Gy gamma irradiation, and with Teng et al.,¹⁵ who observed significant decreases in CAT, glutathione (GSH), and SOD in intestinal tissues after 5 Gy X ray exposure.
Under oxidative stress, Nrf2 becomes activated and translocates to the nucleus, where it induces the expression of detoxifying and antioxidant enzymes, including NQO1, HO 1, SOD, CAT, and GSH related systems.¹⁶ In agreement with these regulatory pathways, our study demonstrated a significant decline in Nrf2 and HO 1 levels in hippocampal homogenates of irradiated rats, consistent with the findings of Teng et al..¹⁵ Conversely, pretreatment with sinapic acid prior to X-ray markedly enhanced Nrf2/HO 1 signaling, restored endogenous antioxidant enzyme activities, and reduced MDA accumulation. These observations parallel the results of Ahmad Ansari et al.,¹⁷ who showed that sinapic acid mitigated 5 fluorouracil induced renal oxidative injury by upregulating Nrf2 and HO 1 and subsequently increasing SOD, GPx, and CAT while lowering MDA and NO.
NF κB serves as a central transcriptional regulator of inflammatory signaling, binding promoter regions of numerous immune related genes and driving the production of cytokines such as TNF α, IL 1β, and IL 6. Earlier work by Li and Karin ¹⁸ showed that ionizing radiation enhances NF κB DNA binding activity through degradation of its cytoplasmic inhibitor IκB α. In agreement with these findings, our results demonstrate that X ray exposure robustly activates NF κB in hippocampal tissue and markedly increases downstream pro inflammatory cytokines. Pretreatment with sinapic acid effectively counteracted these changes, suppressing NF κB activation and normalizing cytokine levels. This anti inflammatory profile is consistent with previous studies: Shahid et al.¹⁹ showed that sinapic acid attenuates colonic inflammation by reducing IL 6 and TNF α expression, while Raish et al.²⁰ reported that it mitigates ethanol induced gastric inflammation through inhibition of NF κB signaling. The ability of sinapic acid to restrain NF κB activation may stem from its capacity to limit ROS generation an established trigger of NF κB as well as its stimulatory effect on the Nrf2 pathway, which is known to exert negative regulatory control over NF κB activity.
Pyroptosis is a highly inflammatory, Caspase 1–dependent form of programmed cell death that culminates in membrane rupture and the release of intracellular pro inflammatory mediators.²¹ Unlike apoptosis, which is primarily mediated by Caspase 3, pyroptosis relies on Caspase 1 activation following assembly of the inflammasome complex.²² A defining feature of this process is the formation of membrane pores that permit cytosolic leakage. The NLRP3–Caspase 1 inflammasome has been identified as a major contributor to radiation induced cellular injury.²³ Ionizing radiation promotes neuronal damage through oxidative stress, inflammatory signaling, and calcium dependent neurotoxicity, largely driven by reactive radicals generated through water radiolysis that attack nucleic acids, lipids, and other intracellular targets.²⁴ Consistent with these mechanisms, our X ray–irradiated rats exhibited pronounced increases in pyroptotic markers (NLRP3, Caspase 1, GSDMD) alongside elevated levels of intrinsic apoptotic proteins, including Caspase 9, cytochrome c, Caspase 3, and Bax. Pretreatment with sinapic acid markedly attenuated both pyroptotic and apoptotic responses in the hippocampus. These findings parallel those of Ali et al.,²⁵ who reported that sinapic acid suppresses inflammasome activation in an epilepsy model, and Bin Jardan et al.,⁶ who demonstrated its anti apoptotic effects in doxorubicin induced cardiotoxicity. The protective effect of sinapic acid against pyroptosis may stem from its ability to limit upstream triggers of inflammasome activation. By reducing oxidative stress and scavenging reactive oxygen species, sinapic acid likely prevents ROS dependent priming of the NLRP3 inflammasome. Additionally, its activation of the Nrf2 pathway may further suppress inflammasome assembly and Caspase 1 activation, thereby reducing GSDMD cleavage and preventing membrane pore formation. Through these combined antioxidant and anti inflammatory actions, sinapic acid effectively interrupts the cascade leading to pyroptotic cell death.

Limitations

The present study has several limitations. Hippocampal injury was evaluated at a single time point (48 h) and with only one radiation dose (8 Gy), precluding assessment of long-term protection or dose-response relationships. Additionally, findings are limited to male Wistar rats, and the lack of specific pathway inhibitors restricts confirmation of causal mechanisms.

Conclusion

This study demonstrates that sinapic acid confers robust neuroprotection against X ray–induced hippocampal injury through a coordinated, multimodal mechanism. Ionizing radiation markedly disrupted the endogenous Nrf2/HO 1 antioxidant system, resulting in excessive oxidative stress, lipid peroxidation, and depletion of key enzymatic defenses. Pretreatment with sinapic acid effectively restored this antioxidant axis, reestablishing redox homeostasis and limiting oxidative damage. In parallel, sinapic acid attenuated radiation evoked neuroinflammation by suppressing NF κB activation and reducing downstream cytokine production. It also inhibited both pyroptotic (NLRP3/Caspase 1/GSDMD) and intrinsic apoptotic (Caspase 9/Caspase 3/Bax/cytochrome c) pathways, thereby preventing programmed cell death. These molecular improvements were reflected histologically by the preservation of CA3 pyramidal neuron morphology.

Declarations

Abbreviations

References

1. Khuntia D, Brown P, Li J, et al. Whole-brain radiotherapy in the management of brain metastasis. J Clin Oncol. 2006;24(8):1295-1304. doi:10.1200/jco.2005.04.6185
   Article · PubMed · Google Scholar
2. Scoccianti S, Detti B, Cipressi S, et al. Changes in neurocognitive functioning and quality of life in adult patients with brain tumors treated with radiotherapy. J Neurooncol. 2012;108(2):291-308. doi:10.1007/s11060-012-0821-8
   Article · PubMed · Google Scholar
3. Farombi EO, Ugwuezunmba MC, Ezenwadu TT, et al. Tetracycline-induced reproductive toxicity in male rats: effects of vitamin C and N-acetylcysteine. Exp Toxicol Pathol. 2008;60(1):77-85. doi:10.1016/j.etp.2008.02.002
   Article · PubMed · Google Scholar
4. Pandi A, Kalappan VM. Pharmacological and therapeutic applications of sinapic acid: an updated review. Mol Biol Rep. 2021;48(4):3733-3745. doi:10.1007/s11033-021-06367-0
   Article · PubMed · Google Scholar
5. Verma V, Singh D, Kh R. Sinapic acid alleviates oxidative stress and neuroinflammatory changes in a sporadic model of Alzheimer disease in rats. Brain Sci. 2020;10(12):923. doi:10.3390/brainsci10120923
   Article · PubMed · Google Scholar
6. Bin Jardan YA, Ansari MA, Raish M, et al. Sinapic acid ameliorates oxidative stress, inflammation, and apoptosis in acute doxorubicin-induced cardiotoxicity via the NF-κB-mediated pathway. Biomed Res Int. 2020;2020:3921796. doi:10.1155/2020/3921796
   Article · PubMed · Google Scholar
7. Lee EH, Shin JH, Kim SS, et al. Sinapic acid controls inflammation by suppressing NLRP3 inflammasome activation. Cells. 2021;10(9):2327. doi:10.3390/cells10092327
   Article · PubMed · Google Scholar
8. Lee JY. Anti-inflammatory effects of sinapic acid on 2,4,6-trinitrobenzenesulfonic acid-induced colitis in mice. Arch Pharm Res. 2018;41(2):243-250. doi:10.1007/s12272-018-1006-6
   Article · PubMed · Google Scholar
9. Ahmad A, Alkharfy KM, Bin Jardan YA, et al. Sinapic acid mitigates methotrexate-induced hepatic injuries in rats through modulation of Nrf2/HO-1 signaling. Environ Toxicol. 2021;36(7):1261-1268. doi:10.1002/tox.23123
   Article · PubMed · Google Scholar
10. Hussein MR, Abu-Dief EE, Abou El-Ghait AT, et al. Morphological evaluation of the radioprotective effects of melatonin against X-ray-induced early and acute testis damage in albino rats: an animal model. Int J Exp Pathol. 2006;87(3):237-250. doi:10.1111/j.1365-2613.2006.00480.x
    Article · PubMed · Google Scholar
11. Lu Z, Zheng X, Ding C, et al. Deciphering the biological effects of radiotherapy in cancer cells. Biomolecules. 2022;12(9):1167. doi:10.3390/biom12091167
    Article · PubMed · Google Scholar
12. Kitagawa T, Yamamoto J, Tanaka T, et al. 5-Aminolevulinic acid strongly enhances delayed intracellular production of reactive oxygen species generated by ionizing irradiation: quantitative analyses and visualization of intracellular reactive oxygen species production in glioma cells in vitro. Oncol Rep. 2015;33(2):583-590. doi:10.3892/or.2014.3618
    Article · PubMed · Google Scholar
13. Zhao M, Wang Y, Li L, et al. Mitochondrial reactive oxygen species promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mitochondrial DNA maintenance. Theranostics. 2021;11(4):1845-1863. doi:10.7150/thno.50905
    Article · PubMed · Google Scholar
14. Erol FS, Topsakal C, Ozveren MF, et al. Protective effects of melatonin and vitamin E in brain damage due to gamma radiation: an experimental study. Neurosurg Rev. 2004;27(1):65-69. doi:10.1007/s10143-003-0291-8
    Article · PubMed · Google Scholar
15. Teng Y, Ma J, Zhang J, et al. X-ray irradiation induces oxidative stress and upregulates the intestinal Nrf2-Mrp2 pathway, leading to decreased intestinal absorption of valsartan. Pharmaceutics. 2025;17(2):268. doi:10.3390/pharmaceutics17020268
    Article · PubMed · Google Scholar
16. Sivandzade F, Prasad S, Bhalerao A, et al. NRF2 and NF-κB interplay in cerebrovascular and neurodegenerative disorders: molecular mechanisms and possible therapeutic approaches. Redox Biol. 2019;21:101059. doi:10.1016/j.redox.2018.11.017
    Article · PubMed · Google Scholar
17. Ahmad Ansari M, Shahid M, Ahmad SF, et al. Sinapic acid alleviates 5-fluorouracil-induced nephrotoxicity in rats via Nrf2/HO-1 signalling. Saudi Pharm J. 2023;31(7):1351-1359. doi:10.1016/j.jsps.2023.05.021
    Article · PubMed · Google Scholar
18. Li N, Karin M. Is NF-κB the sensor of oxidative stress? FASEB J. 1999;13(10):1137-1143. doi:10.1096/fasebj.13.10.1137
    Article · PubMed · Google Scholar
19. Shahid M, Raish M, Ahmad A, et al. Sinapic acid ameliorates acetic acid-induced ulcerative colitis in rats by suppressing inflammation, oxidative stress, and apoptosis. Molecules. 2022;27(13):4139. doi:10.3390/molecules27134139
    Article · PubMed · Google Scholar
20. Raish M, Shahid M, Bin Jardan YA, et al. Gastroprotective effect of sinapic acid on ethanol-induced gastric ulcers in rats: involvement of Nrf2/HO-1 and NF-κB signaling and an antiapoptotic role. Front Pharmacol. 2021;12:622815. doi:10.3389/fphar.2021.622815
    Article · PubMed · Google Scholar
21. LaRock CN, Cookson BT. Burning down the house: cellular actions during pyroptosis. PLoS Pathog. 2013;9(12). doi:10.1371/journal.ppat.1003793
    Article · PubMed · Google Scholar
22. Aachoui Y, Sagulenko V, Miao EA, et al. Inflammasome-mediated pyroptotic and apoptotic cell death and defense against infection. Curr Opin Microbiol. 2013;16(3):319-326. doi:10.1016/j.mib.2013.04.004
    Article · PubMed · Google Scholar
23. Ortiz F, Acuña-Castroviejo D, Doerrier C, et al. Melatonin blunts the mitochondrial/NLRP3 connection and protects against radiation-induced oral mucositis. J Pineal Res. 2015;58(1):34-49. doi:10.1111/jpi.12191
    Article · PubMed · Google Scholar
24. Weiss JF, Kumar KS. Antioxidant mechanisms in radiation injury and radioprotection. In: Cellular Antioxidant Defense Mechanisms. CRC Press; 2019:163-190. doi:10.1201/9780429289309-10
    Article · PubMed · Google Scholar
25. Ali SO, Ghaiad HR, Elmasry GF, et al. Sinapic acid mitigates pentylenetetrazol-induced acute seizures by modulating the NLRP3 inflammasome and regulating calcium/calcineurin signaling: in vivo and in silico approaches. Inflammation. 2024;47(6):1969-1986.Lu Z, Zheng X, Ding C, et al. Deciphering the biological effects of radiotherapy in cancer cells. Biomolecules. 2022;12(9):1167. doi:10.1007/s10753-024-02019-0
    Article · PubMed · Google Scholar

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